Whether saturated fat is a risk factor for cardiovascular disease (CVD) is a question with numerous controversial views.[1] Although most in the mainstream heart-health, government, and medical communities hold that saturated fat is a risk factor for CVD, some recent studies have produced conflicting results.

In 2014, a systematic review and meta-analysis in the Annals of Internal Medicine, of 72 published studies totalling 530,525 participants, looked at observational studies of dietary intake of fatty acids, observational studies of measured fatty acid levels in the blood, and intervention studies of polyunsaturated fat supplementation. The authors of the review concluded that, ″Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.″[12]

However, Walter Willett, chair of the Department of Nutrition at Harvard School of Public Health, warns that the conclusions are seriously misleading, as the analysis contains major errors and omissions. Dr. Willett emphasized that because this meta-analysis contains multiple serious errors and omissions, the study conclusions are misleading and should be disregarded.[23]

″The meta-analysis of dietary fatty acids and risk of coronary heart disease by Chowdhury et al. contains multiple errors and omissions, and the conclusions are seriously misleading, particularly the lack of association with N-6 polyunsaturated fat. For example, two of the six studies included in the analysis of N-6 polyunsaturated fat were wrong. The relative risks for Nurses’ Health Study (NHS) and Kuopio Ischemic Heart Disease Study (KIHD) were retrieved incorrectly and said to be above 1.0. However, in the 20-year follow-up of the NHS the relative risk for highest vs lowest quintile was 0.77 (95 percent CI: 0.62, 0.95); ptrend = 0.01 (the authors seem to have used the RR for N-3 alpha-linolenic acid from a paper on sudden cardiac death), and in the KIHD the relative risk was 0.39; 95% confidence interval [CI], 0.21-0.71) (the origin of the number used in the meta-analysis is unclear). Also, relevant data from other studies were not included.

Further, the authors did not mention a pooled analysis of the primary data from prospective studies, in which a significant inverse association between intake of polyunsaturated fat (the large majority being the N-6 linoleic acid) and risk of CHD was found. Also, in this analysis, substitution of polyunsaturated fat for saturated fat was associated with lower risk of CHD. Chowdhury et al. also failed to point out that most of the monounsaturated fat consumed in their studies was from red meat and dairy sources, and the findings do not necessarily apply to consumption in the form of nuts, olive oil, and other plant sources. Thus, the conclusions of Chowdhury et al. regarding the type of fat being unimportant are seriously misleading and should be disregarded.″

In a 2013 systematic review in the American Journal of Cardiovascular Disease, Fred Kummerow relays information about the role of oxidized LDL and the role of saturated and poly-unsaturated fats role in the formation of atherosclerosis. He shows two studies where polyunsaturated fats are the main contributor to atherosclerosis and coronary heart disease.[24]

A 2011 systematic review from The Cochrane Library analyzed 48 studies conducted between 1965 and 2009 and included 65,508 participants. All studies reduced or modified participants’ dietary fat or cholesterol for at least six months by at least 30 percent. It was found that reducing saturated fat by reducing and/or modifying dietary fat reduced the risk of having a cardiovascular event, such as heart attack, stroke and unplanned heart surgery, by 14 percent. Of the 65,508 participants, 7 percent had a cardiovascular event.

"The findings are suggestive of a small but potentially important reduction in cardiovascular risk on modification of dietary fat, but not reduction of total fat, in longer trials. Lifestyle advice to all those at risk of cardiovascular disease and to lower risk population groups, should continue to include permanent reduction of dietary saturated fat and partial replacement by unsaturates. The ideal type of unsaturated fat is unclear". In a summary it goes on to say "there are no clear health benefits of replacing saturated fats with starchy foods".[13]

In a subordinate meta-analysis to a 2009 risk assessment supported by the Centers for Disease Control and Prevention (CDC), an ischemic heart disease mortality residual risk of 1.05 was determined for the 30-44 year age group for each 1% isocaloric reduction in PUFA in favour of SFA. Higher age groups had lower residual risks.[15]

In 2009, a systematic review supported by the Heart and Stroke Foundation of Canada of prospective cohort studies or randomized trials concluded that there was "insufficient evidence of association" between intake of saturated fatty acids and coronary heart disease, and pointed to strong evidence for protective factors such as vegetables and a Mediterranean diet and harmful factors such as trans fats and foods with a high glycemic index.[16]

A 2009 meta-analysis supported by the NHBLI focused on the effects of trans-fats also applied the same techniques to studies focused on SFA, MUFA and PUFA, in order to assess the relative risk of substituting trans-fats with other fats. Risks were assessed from two classes of data - risk factors in trials, and disease outcomes in cohort studies. In order of decreasing risk, the fat types were TFA, SFA, MUFA and PUFA. From the trials analysis, it was found that for partially hydrogenated vegetable oil with 20% trans-fats at consumption rate of 7.5% of daily calories, replacement with butter would decrease risk by 2.7% and replacement with canola oil would reduce risk by 9.9%. From the cohort analysis, butter would have little net effect (0.5% increased risk) while soybean and canola oil would have the largest reduction in risk (19.0 and 21.8%, respectively).[28]

A 2009 meta-analysis of cohort studies and randomized controlled trials from the University of Otago, New Zealand, found that the results of the cohort studies showed no association between coronary heart disease mortality nor total coronary heart disease events when saturated fat was increased in place of carbohydrates. In the randomized controlled trials where the ratio of polyunsaturated fat to saturated fat had been increased, the risk of coronary heart disease fatality was not changed, but the risk of total coronary heart disease events was decreased. The analysis was critical of the limitations of the primary evidence available, considering the evidence from cohort studies to be mostly unreliable.[17]

A 2009 pooled analysis of 11 cohort studies supported by the National Heart, Lung, and Blood Institute, National Institutes of Health, the Danish Heart Foundation and the Danish Medical Research Council found that substituting polyunsaturated fatty acids in place of saturated fatty acids at a rate of 5% of energy intake led to 13% decrease in coronary events and a 26% decrease in coronary deaths.[18]

The American Dietetic Association's 2008 systematic review found that a diet with 25%-35% total fat but less than 7% saturated fat and trans fat lowers the risk of coronary heart disease.[19]

A 2003 meta-analysis of prevention dietetic studies found the benefit of a modified fat diet in primary prevention is potentially significant if it is maintained for a sufficient length of time.[20]

A 1999 review found that substitution of the fat from one ounce of nuts for equivalent energy from saturated fat was associated with a 45% reduction in risk of coronary heart disease.[21]

A 1994 meta-analysis from the University of Sydney of the effect on coronary events and total mortality in dietary intervention trials found a 6% reduction in mortality and 13% reduction in events. The dietary advice differed between the trials reviewed, but most prescribed a reduced saturated fat and cholesterol intake with partial replacement by polyunsaturated oils. The review noted that a large controlled trial "may no longer be ethical."[22]

Some meta-analyses have found a significant relationship between saturated fat and serum cholesterol levels, and serum cholesterol levels and cardiovascular disease. However, the ratio of total to high density lipoprotein cholesterol is considered a better indicator and some saturated fats (lauric acid and stearic acid) improve the ratio.[29][30][31]

The 2009 European Society of Cardiology Textbook of Cardiovascular Medicine states that in cohort studies the positive relationship between fat intake and CVDs was linked to their saturated fatty acid content.[32]

2007's Cardiovascular Prevention and Rehabilitation states that large epidemiological studies have shown consistent associations between the intake of saturated fatty acids and CHD mortality.[33]

According to the 2007 Critical Pathways in Cardiovascular Medicine, substituting unsaturated fat for saturated fat may lower LDL cholesterol without simultaneously lowering HDL cholesterol. This dietary principle partly underlies the Mediterranean style of diet, which has been associated with reduced cardiovascular event rates in two randomized controlled trials.[34]

The 2003 second edition of Evidence-based Cardiology in 'PartII: Prevention of cardiovascular diseases' recommends a low intake of SFA, less than 7% of daily calories, and intake of foods rich in myristic and palmitic acids should be especially reduced. The recommendation was evaluated to be supported by the best grade of available evidence.[35]

Position statements and guidelines of major health organizations[edit]

In 2003 a World Health Organization (WHO) and Food and Agricultural Organization (FAO) expert consultation report concluded that "intake of saturated fatty acids is directly related to cardiovascular risk. The traditional target is to restrict the intake of saturated fatty acids to less than 10%, of daily energy intake and less than 7% for high-risk groups. If populations are consuming less than 10%, they should not increase that level of intake. Within these limits, intake of foods rich in myristic and palmitic acids should be replaced by fats with a lower content of these particular fatty acids. In developing countries, however, where energy intake for some population groups may be inadequate, energy expenditure is high and body fat stores are low (BMI <18.5 kg/m2). The amount and quality of fat supply has to be considered keeping in mind the need to meet energy requirements. Specific sources of saturated fat, such as coconut and palm oil, provide low-cost energy and may be an important source of energy for the poor."[36]

In its 2007 guidelines, the European Society of Cardiology states that there are strong, consistent, and graded relationships between saturated fat intake, blood cholesterol levels, and the mass occurrence of cardiovascular disease. The relationships are accepted as causal.[37]

The Mayo Clinic considers saturated fats potentially harmful and monounsaturated and polyunsaturated fats potentially helpful. It references the Dietary Guidelines for Americans, 2010 and recommends reducing foods rich in saturated fat and emphasizing options with more monounsaturated and polyunsaturated fats.[38]

The British Dietetic Association guidelines found good evidence in systematic reviews of randomized controlled trials that reducing saturated fat reduces morbidity in patients with CVD.[39]

The 2007 position statement of the American Dietetic Association and the Dieticians of Canada holds that epidemiological studies have shown a positive association between the intake of saturated fatty acid and the incidence of coronary heart disease.[3]

Consumption of saturated fat is a risk factor for cardiovascular disease in the view of the Canadian Heart and Stroke Foundation,[40] the American Heart Association,[41] the British Heart Foundation,[6] the National Heart Foundation of Australia,[42] the National Heart Foundation of New Zealand [43] and the World Heart Federation.[7] The Irish Heart Foundation states that saturated fats can raise your LDL cholesterol and increase your chances of getting heart disease.[44]

The Dietary Guidelines for Americans, 2010 produced by the U.S. Department of Agriculture (USDA) and U.S. Department of Health and Human Services says the human body makes more than enough saturated fats to meet its needs and does not require more from dietary sources. It says higher levels of saturated fats are associated with higher levels of total cholesterol and low-density lipoprotein "bad" cholesterol and recommends reduced saturated fat intake.[45] The guidelines are based on the recommendations of the Dietary Guidelines Advisory Committee (DGAC) report that incorporated the results of the review of 12 studies from 2004 to 2009 conducted by the Nutrition Evidence Library (NEL) part of the Evidence Analysis Library Division of the USDA's Center for Nutrition Policy and Promotion. The NEL concluded that there was "strong" evidence that dietary saturated fats increased serum total cholesterol and LDL cholesterol and increased risk of cardiovascular disease.[46][47]

A May 2011 extended feature in the Journal of the American Dietetic Association published an edited summary of a debate at the American Dietetic Association's 93rd conference. Regarding saturated fat, the key point agreed upon by the panel and scientific community at large was that "Researchers agree that replacing saturated fat with healthy PUFAs is beneficial for health and [cardiovascular disease]." Recommendations for dieticians emphasized using mono- and poly-unsaturated fats whenever possible, avoiding trans fats, that while "The evidence against saturated fat may not be as strong as dietary guidelines have interpreted [it is clear] that PUFAs (especially) and MUFAs are healthy fats", and that while there is room for saturated fats within the diet but "[they] should not be viewed as good for you".[48]

It also noted "dietary patterns are more important than single dietary components" and recommended dietitians "to talk food, not chemicals".[48]

A 2010 perspective in the American Journal of Clinical Nutrition found that the risk of coronary heart disease (CHD) is reduced when saturated fatty acids are replaced with polyunsaturated fatty acids but no clear benefit in replacing saturated fatty acids with carbohydrates or monounsaturated fatty acids.[49]

In an October 2010 article in the journal Nutrition, the 2010 Dietary Guidelines Advisory Committee (DGAC) report was criticized for the "use of an incomplete body of relevant science; inaccurately representing, interpreting, or summarizing the literature; and drawing conclusions and/or making recommendations that do not reflect the limitations or controversies in the science" stating rather that the evidence associating dietary SFA with increased risk of CVD is inconclusive.[50]

A response by Jeremiah Stamler to the 2010 meta-analysis by Siri-Tarino et al.[1] was point-by-point critical of the analysis, stating "The authors are inaccurate in concluding that 'there are few epidemiologic or clinical trial data to support a benefit of replacing saturated fat with carbohydrate.'" and questioned if it was the intent to dissociate themselves from prevailing recommendations, "A vast array of concordant multidisiplinary research evidence is the sound foundation for these recommendations."[51]

A 2009 review from the University of São Paulo found that the best evidence showed reduced intake of saturated fat decreased risk for coronary heart disease.[52]

A 2009 review from King's College London found that epidemiological evidence suggested a negative influence on vascular function from saturated fat, but that the experimental evidence did not support this convincingly.[53]

A 2009 scientific conference hosted by the University of Reading (UK) and organized and facilitated by the International Dairy Federation’s Standing Committee on Nutrition and Health found that despite the contribution of dairy products to the saturated fatty acid intake of the diet, there was no clear evidence that dairy food consumption is consistently associated with a higher risk of CVD.[54]

A 2004 commentary from the Nestle Research Center stated that no randomized clinical trials of low-fat diets or low-saturated fat diets of sufficient duration had been carried out. The influence of varying saturated fatty acid intakes against a background of different individual lifestyles and genetic backgrounds were recommended as the focus in future studies.[55] Saturated fat intakes may be monitored more closely than were total fat intakes, therefore ignoring the possibility that simply a larger fat intake may lead to a higher risk of coronary diseases. It also suggests that other parameters may be overlooked, such as carbohydrates intakes.[56]

A 2000 consensus statement appearing in The American Journal of Medicine listed in factors important to prevent heart disease a substantial reduction of saturated fat and partially hydrogenated oils, and the substitution of saturated fats by unsaturated fats.[57]

Author and journalist Michael Pollan, a two-time James Beard Foundation Award winner, in his book In Defense of Food – An Eater's Manifesto states "The amount of saturated fat in the diet probably may have little if any bearing on the risk of heart disease, and evidence that increasing polyunsaturated fats in the diet will reduce risk is slim to nil."[60]

Michael Shermer Editor of Sceptic Magazin says on face book:" Michael Shermer den 3 juli 2014 · Nina Teicholz's book is a good read & she did her homework showing that the diet-cholesterol-heart disease connection is not that solid. [63] Östen Örbrink

The Dairy Farmers of Canada quote Andrew Mente, PhD (Assistant Professor, Department of Clinical Epidemiology and Biostatistics, McMaster University) that "In light of new scientific data, it appears that saturated fat is not associated with an increased risk of cardiovascular disease."[64]

^ abZelman, K. (2011). "The Great Fat Debate: A Closer Look at the Controversy—Questioning the Validity of Age-Old Dietary Guidance". Journal of the American Dietetic Association111 (5): 655–658. doi:10.1016/j.jada.2011.03.026. PMID21515106.edit